Diğer Açık Erişim

Expressions of the satellite repeat HSAT5 and transposable elements are implicated in disease progression and survival in glioma (Supplementary Files)

Köse, Sıla Naz; Yaraş, Tutku; Bursalı, Ahmet; Oktay, Yavuz; Yandım, Cihangir; Karakülah, Gökhan


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    <subfield code="a">&lt;p&gt;The glioma genome encompasses a complex array of dysregulatory events, presenting a formidable challenge in managing this devastating disease. Despite the widespread distribution of repeat and transposable elements across the human genome, their involvement in glioma&amp;#39;s molecular pathology and patient survival remains largely unexplored. In this study, we aimed to to characterize the links between the expressions of repeat / transposable elements with disease progression and survival in glioma patients. Hence, we analyzed the expression levels of satellite repeats and transposons along with genes in low-grade glioma (LGG) and high-grade glioma (HGG). Endogenous transposable elements LTR5 and HERV_a-int exhibited higher expression in HGG patients, along with immune response-related genes. Altogether, 16 transposable elements were associated with slower progression of disease in LGG patients. Conversely, 22 transposons and the HSAT5 satellite repeat were linked to a shorter event-free survival in HGG patients. Intriguingly, our weighted gene co-expression network analysis (WGCNA) disclosed that the HSAT5 satellite repeat resided in the same module network with genes implicated in chromosome segregation and nuclear division; potentially hinting at its contribution to disease pathogenesis. Collectively, we report for the first time that repeat and/or transposon expression could be related to disease progression and survival in glioma. The expressions of these elements seem to exert a protective effect during LGG-to-HGG progression, whereas they could have a detrimental impact once HGG is established. The results presented herein could serve as a foundation for further experimental work aimed at elucidating the molecular regulation of glioma genome.&lt;/p&gt;</subfield>
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